FIG. 1 depicts a human heart 100. As can be seen from FIG. 1, the heart 100 includes four chambers, the right and left atria 102 and 104, respectively, and the right and left ventricles 106 and 108, respectively. The heart 100 pumps so as to circulate blood through the human body in the following manner. Blood flows from the peripheral venous system to the right atrium 102. From the right atrium 102, blood passes through the tricuspid valve 110 to the right ventricle 106. Blood exits the right ventricle 106 through the pulmonary artery and is directed through the lungs, so that the blood may be reoxygenated. Oxygenated blood from the lungs is drawn from the pulmonary vein to the left atrium 104. From the left atrium, blood passes though the mitral valve 112 to the left ventricle 108. Finally, the blood flows from the left ventricle 108, through the aortic valve, to the peripheral arterial system in order to transfer oxygenated blood to the organs of the body.
To cause the blood to circulate in the above-described manner, electrical pulses propagate through the heart 100, causing the various cardiac muscle cells to contract when excited by the pulses. Usually, the cycle of electrical excitation of the heart 100 is initiated by the sinoatrial node 114. An electrical impulse is generated by the sinoatrial node 114. The impulse propagates from the sinoatrial node 114 to the right and left atria 102 and 104. As a consequence of normal propagation, the right and left atria 102 and 104 contract at substantially the same time. Contraction of the atria 102 and 104 force blood from the right and left atria 102 and 104 into the right and left ventricles 106 and 108, respectively. Eventually, the electrical impulse reaches the atrioventricular node 116. From the atrioventricular node 116, the electrical impulse is carried along right and left bundle branch fibers (not depicted) to a network of fast-conducting Purkinje fibers (not depicted) that extend throughout most of the endocardial surface of the ventricles 106 and 108. The ventricles 106 and 108, when excited by the electrical impulse, contract at substantially the same time, causing the blood therein to exit and travel to either the lungs or the peripheral arterial system, as mentioned above.
Efficiency of heart function may be influenced by several factors. Amongst those factors is synchrony between the chambers of the heart. Efficient heart function is encouraged by atrio-ventricular synchrony, meaning that the ventricles 106 and 108 should contract shortly after contraction of the atria 102 and 104. Premature ventricular contraction may lead to inefficiency because the ventricles 106 and 108 do not become fully filled with blood before contraction. On the other hand, retarded ventricular contraction may permit some of the blood contained in the ventricles 106 and 108 to flow back into the atria 102 and 104 prior to ventricular contraction—an effect that is also inimical to efficient heart function.
Efficient heart function is also encouraged by interventricular synchrony. The right and left ventricles 106 and 108 share a wall in common, the septum 118. Should the right ventricle 106 contract prior to contraction of the left ventricle 108, the septum 118 may initially contract with the right ventricle 106, shifting to the right. Then, upon contraction of the left ventricle 108, the septum 118 may contract with the left ventricle 108, and shift to the left. Thus, the septum 118 may exhibit a sort of “waffling” action, shifting first to the right and then to the left. Such waffling yields an inefficient cardiac stroke.
To encourage proper synchrony amongst the ventricles 106 and 108 or atria 102 and 104, cardiac resynchronization therapy may be employed by a cardiac rhythm management device, such as a pacemaker or defibrillator with pacing capabilities. Herein, the terms pacemaker, pulse generator device, and cardioverter/defibrillator (with pacing functionality) are used interchangeably and refer to an cardiac rhythm management device. Cardiac resynchronization therapy involves pacing one or both ventricles 106 and 108 in order to synchronize their contraction with one another or with one or both of the atria 102 and 104.
One important variable governing cardiac resynchronization therapy is an atrio-ventricular pacing delay interval that is employed by the device applying the resynchronization therapy. As explained in more detail, below, the atrio-ventricular pacing delay interval is responsible for determining the timing of pacing of one or both of the ventricles relative to a paced or sensed event occurring in the right atrium 102.
In atrial tracking and AV sequential pacing modes, a ventricular escape interval is defined between atrial and ventricular events. This escape interval is the aforementioned atrio-ventricular pacing delay interval or AVD interval, where a ventricular pacing pulse is delivered upon expiration of the atrio-ventricular pacing delay interval if no ventricular sense occurs before such expiration. In an atrial tracking mode, the atrio-ventricular pacing delay interval is triggered by an atrial sense and stopped by a ventricular sense or pace. An atrial escape interval can also be defined for pacing the atria either alone or in addition to pacing the ventricles. In an AV sequential pacing mode, the atrio-ventricular delay interval is triggered by an atrial pace and stopped by a ventricular sense or pace. Atrial tracking and AV sequential pacing are commonly combined so that the AVD interval starts with either an atrial pace or sense.